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Abstract
Humans who have inherited the human class I major histocompatibility allele HLA-B27
have a markedly increased risk of developing the multi-organ system diseases termed
spondyloarthropathies. To investigate the role of B27 in these disorders, we introduced
the B27 and human beta 2-microglobulin genes into rats, a species known to be quite
susceptible to experimentally induced inflammatory disease. Rats from one transgenic
line spontaneously developed inflammatory disease involving the gastrointestinal tract,
peripheral and vertebral joints, male genital tract, skin, nails, and heart. This
pattern of organ system involvement showed a striking resemblance to the B27-associated
human disorders. These results establish that B27 plays a central role in the pathogenesis
of the multi-organ system processes of the spondyloarthropathies. Elucidation of the
role of B27 should be facilitated by this transgenic model.